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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A previous study showed a strong relationship between human focal epilepsy and the presence in the cortex of "activated" astrocytes characterized by an intense activity of dehydrogenases (DH) involved in glucose metabolism and of glutamate DH. Using the semi-chronic model of cobalt-induced experimental focal epilepsy in the rat, we investigated a possible correlation between astrocyte modifications and the chronological development of the epileptic manifestations on the ECoG. After a few days the cobalt-implanted rats present spikes, then sharp waves followed by an electrical crisis and ultimately motor seizures. Activated astrocytes were found in each phase of this evolution. Their number increases with the intensity of the manifestations. There is a close relationship between activated astrocytes and focal epileptic phenomena. At this stage of our study it is clear that the presence of activated astrocytes is not a consequence of seizures. However, it is impossible to say whether the activation is secondary to the hyperactivity of the neurons or directly responsible for the constitution of the epileptic focus. In any case, activated astrocytes provide a new means of localizing an epileptogenic focus.
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PMID:Histochemical study of cobalt-induced focal epilepsy. 9 27

The mechanisms of the anticonvulsant activity of cannabidiol (CBD) and the central excitation of delta 9-tetrahydrocannabinol (delta 9-THC) were investigated electrophysiologically with conscious, unrestrained cobalt epileptic rats. The well-known antiepileptics, trimethadione (TMO), ethosuximide (ESM), and phenytoin (PHT), were included as reference drugs. Direct measurements were made of spontaneously firing, epileptic potentials from a primary focus on the parietal cortex and convulsions were monitored visually. ESM and TMO decreased the frequency of focal potentials, but PHT and CBD exerted no such effect. Although CBD did not suppress the focal abnormality, it did abolish jaw and limb clonus; in contrast, delta 9-THC markedly increased the frequency of focal potentials, evoked generalized bursts of polyspikes, and produced frank convlusions. 11-OH-delta 9-THC, the major metabolite of delta 9-THC, displayed only one of the excitatory properties of the parent compound: production of bursts of polyspikes. In contrast to delta 9-THC and its 11-OH metabolite, CBD, even in very high doses, did not induce any excitatory effects or convulsions. The present study provides the first evidence that CBD exerts anticonvulsant activity against the motor manifestations of a focal epilepsy, and that the mechanism of the effect may involve a depression of seizure generation or spread in the CNS.
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PMID:The influence of cannabidiol and delta 9-tetrahydrocannabinol on cobalt epilepsy in rats. 11 6

The present work addresses itself to answering several questions in relations to the antiepileptic action of taurine (see "Introduction"). For this purpose, cobalt epileptic mice, treated with isoosmolar saline or not treated, was compared with groups of mice that had received doses of taurine varying between 1.0 and 10.0 mg/kg. Whereas all the taurine doses employed effectively reduced seizure incidence, with 10.0 mg/kg giving the best results, none of these doses had ameliorated the amino acid abnormalities in the cortex after two days of treatment in comparison with the group that had received isoosmolar saline. On the contrary, the largest amino acid abnormalities occurred in the group of mice (10.0 mg/kg) that had improved the most clinically. We conclude that the acute antiseizure action of taurine, and its effect on restoring normal amino acid patterns in the cortex, represent two separate properties of taurine.
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PMID:Influence of taurine dosage on cobalt epilepsy in mice. 68 11

In rats with cobalt implanted in the right frontal cerebral cortex, acetylcholine (ACh) levels were depressed in the visually non-necotic, surrounding cortex at 7 and 14 days after surgery in comparison with values for controls treated with glass. At 21 days post-implantation, ACh levels were not different for glass and cobalt treatments. Effects of drugs affecting cholinergic function on electro-corticographic (ECoG) epileptiform activity were determined in rats implanted bilaterally with cobalt. The cholinesterase inhibitors, physostigmine and diisopropylfluorophosphate reduced both seizure activity and interictal spiking in these cobalt-treated rats. Hemicholinium-3 (HC-3), given subacutely initially inhibited seizures, but seizure frequency increased later during treatment. HC-3 did not appear to inhibit interictal spiking. These results suggest an involvement of brain cholinergic system in chronic cobalt experimental epilepsy. Seven days after cobalt implantation, HC-3 was less effective in depleting ACh in cerebral cortex adjacent to the cobalt-lesion than in similar tissue from rats with no cobalt implants. This suggests that the cholinergic neurons adjacent to the implant are not highly active at a time when seizure frequency is maximal.
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PMID:Cholinergic involvement in cobalt-induced epilepsy in the rat. 91 28

The effect od dipropylacetic acid (DPA; Depakine) on the bemegride-induced convulsive threshold was investigated in alert cats. Forty-five min after DPA 200 mg/kg, s.c., no significant effect was obtained; 5 min after the same dose iv., protection from bemegride-induced seizures was pronounced. DPA did not decrease focal discharges in sensorimotor cortex produced by topical cobalt, although spread of epileptogenic activity from the focus was inhibited. DPA antiepileptic protection tested by the same procedure was about the same as that given by phenobarbital and less than that given by diazepam.
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PMID:Dipropylacetic acid (Depakine) in experimental epilepsy in the alert cat. 112

The role of the cerebral ganglia in the switching of the behavior of a mollusc from free swimming to hunting behavior was studied. For this purpose the bodies of neurons providing processes to sensory and motor nerves were stained by means of retrograde axonal transport of Co2+ ions, and the behavioral reactions occurring during extracellular stimulation of particular regions of the ganglia were investigated. Comparison of the morphological data with the behavioral reactions showed that the cerebral neurons participate on the basis of sensory information in the switching of quiet swimming to one of three modes: hunting behavior (including the seizure of food), active avoidance, and passive-defensive behavior.
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PMID:Role of the cerebral ganglia in the organization of alimentary behavior of the pteropod mollusc Clione limacina. 138 Jun 78

This paper reviews chemical models of epilepsy and their relevance in the identification and characterization of anticonvulsants. For each convulsant we discuss possible modes of administration, clinical type(s) of seizures induced, proposed mechanism(s) of epileptogenesis and, where available, responsiveness of the induced seizures to anticonvulsants. The following compounds are reviewed: pentylenetetrazol, bicuculline, penicillin, picrotoxin, beta-carbolines, 3-mercaptopropionic acid, hydrazides, allylglycine; the glycine antagonist strychnine; gamma-hydroxybutyrate; excitatory amino acids (glutamate, aspartate, N-methyl-D-aspartate, quisqualate, kainate, quinolinic acid); monosubstituted guanidino compounds, metals (alumina, cobalt, zinc, iron); neuropeptides (opioid peptides, corticotropin releasing factor, somatostatin, vasopressin); cholinergic agents (acetylcholine, acetylcholinesterase inhibitors, pilocarpine); tetanus toxin; flurothyl; folates; homocysteine and colchicine. Although there are a multitude of chemical models of epilepsy, only a limited number are applied in the routine screening of potential anticonvulsants. Some chemical models have a predictive value with regard to the clinical profile of efficacy of the tested anticonvulsants. Some chemical models may contribute to a better understanding of possible mechanisms of epileptogenesis.
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PMID:Chemical models of epilepsy with some reference to their applicability in the development of anticonvulsants. 139 44

The efficacy of valproic acid (VPA) in control of generalized convulsive status epilepticus was tested in a rat model. Rats with cortical cobalt lesions were injected with homocysteine thiolactone to induce secondarily generalized tonic-clonic seizures (GTCS). The median effective dose (ED50) for control of GTCS was 211.9 mg/kg (270 micrograms/ml in serum 30 min post dose) when treatment was given intraperitoneally after the second GTCS. VPA entered both serum and brain very rapidly after injection, with little change in concentration from 5 to 30 min post dose. In earlier experiments with phenytoin, phenobarbital, diazepam and lorazepam in this model, we found that the serum concentrations produced by the ED50s versus GTCS were very similar to those which have been reported to be effective in treating human status epilepticus. If this same relationship holds true for VPA, we would predict that a serum concentration of around 270 micrograms/ml VPA would be required for control of generalized convulsive status epilepticus in human patients. The safety of this high a concentration of VPA has not been tested.
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PMID:Valproic acid treatment of experimental status epilepticus. 139 45

Changes in the strength of recurrent inhibition in the feline cortex in cobalt (CoCl2)-induced epilepsy were observed. The strength of inhibition was analyzed in terms of paired-pulse depression of the amplitude of somatosensory evoked potentials (SEPs) elicited by stimulation of the ventral posterolateral (VPL) thalamic nucleus. An enhancement in recurrent inhibition was observed shortly after CoCl2 application. The size of the amplitude of cortical evoked potentials (EPs) elicited by VPL stimulation increased simultaneously. The reduction of inhibition that appeared later was associated with afterdischarges (ADs) evoked by VPL stimulation. These ADs frequently extended to epileptic discharges. These results suggest that the reduction in recurrent inhibition induced by CoCl2 application plays an important role in the spread of seizure activity.
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PMID:Changes in the strength of recurrent inhibition in cobalt-induced epilepsy. 159 15

Adult female Sprague-Dawley rats rendered epileptic by bilateral cerebral implantation of cobalt wire were simultaneously prepared with permanent cortical and temporalis muscle electrodes for continuous recording of electroencephalogram and electromyogram activities. Carbamazepine (50 or 100 mg/kg) was administered intraperitoneally twice daily days 8-12 after cobalt implantation. The high dose of carbamazepine was effective in decreasing seizure incidence each day of its administration, but the lower dose was effective in decreasing seizure incidence only for 6 h following its administration on days 8 and 9. These results provide additional evidence that cobalt epilepsy in the rat is a valid model for the study of seizure disorders.
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PMID:Reduction of frequency of seizures by carbamazepine during cobalt experimental epilepsy in the rat. 159 49


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